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However, reperfusion after angioplasty represents a clinical paradox, restoring blood flow to the ischemic myocardium while simultaneously inducing ion and metabolic imbalances that stimulate immune cell recruitment and activation, mitochondrial dysfunction and damaging oxidant production.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Advances:<\/jats:title>\n                    <jats:p>Preclinical data indicate that these metabolic imbalances contribute to subsequent heart failure through sustaining local recruitment of inflammatory leukocytes and oxidative stress, cardiomyocyte death, and coronary microvascular disturbances, which enhance adverse cardiac remodeling. Both left ventricular dysfunction and heart failure are strongly linked to inflammation and immune cell recruitment to the damaged myocardium.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Critical Issues:<\/jats:title>\n                    <jats:p>Overall, therapeutic anti-inflammatory and antioxidant agents identified in preclinical trials have failed in clinical trials.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Future Directions:<\/jats:title>\n                    <jats:p>The versatile neutrophil-derived heme enzyme, myeloperoxidase (MPO), is gaining attention as an important oxidative mediator of reperfusion injury, vascular dysfunction, adverse ventricular remodeling, and atrial fibrillation. Accordingly, there is interest in therapeutically targeting neutrophils and MPO activity in the setting of heart failure. Herein, we discuss the role of post-AMI inflammation linked to myocardial damage and heart failure, describe previous trials targeting inflammation and oxidative stress post-AMI, highlight the potential adverse impact of neutrophil and MPO, and detail therapeutic options available to target MPO clinically in AMI patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/ars.2019.7928","type":"journal-article","created":{"date-parts":[[2020,6,10]],"date-time":"2020-06-10T03:36:41Z","timestamp":1591760201000},"page":"689-712","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":52,"title":["Neutrophil-Mediated Cardiac Damage After Acute Myocardial Infarction: Significance of Defining a New Target Cell Type for Developing Cardioprotective Drugs"],"prefix":"10.1177","volume":"33","author":[{"given":"Mary","family":"El Kazzi","sequence":"first","affiliation":[{"name":"Discipline of Pathology, Charles Perkins Centre, Sydney Medical School, The University of Sydney, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin Saul","family":"Rayner","sequence":"additional","affiliation":[{"name":"The Heart Research Institute, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Belal","family":"Chami","sequence":"additional","affiliation":[{"name":"Discipline of Pathology, Charles Perkins Centre, Sydney Medical School, The University of Sydney, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanne Marie","family":"Dennis","sequence":"additional","affiliation":[{"name":"Discipline of Pathology, Charles Perkins Centre, Sydney Medical School, The University of Sydney, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shane Ross","family":"Thomas","sequence":"additional","affiliation":[{"name":"Department of Pathology, School of Medical Sciences, The University of New South Wales, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul Kenneth","family":"Witting","sequence":"additional","affiliation":[{"name":"Discipline of Pathology, Charles Perkins Centre, Sydney Medical School, The University of Sydney, Sydney, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2020,8,27]]},"reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2013.01.287"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1096\/fj.05-3718com"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.3390\/antiox8090414"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M101447200"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacbts.2016.09.004"},{"key":"e_1_3_2_7_2","first-page":"1","article-title":"Hypochlorous acid generated in the heart following acute ischaemic injury promotes myocardial damage: a new target for therapeutic development","volume":"9","author":"Alrabadi N","year":"2014","unstructured":"Alrabadi N, , Chami B, , Kim HB, , Maw AM, , Dennis JM, , and Witting PK. 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